title: Ischemia/reperfusion injury to the ileum does not account for the ileal VO2-DO2 alterations induced by endotoxin.
abstract: OBJECTIVE
  Endotoxin (lipopolysaccharide [LPS])-induced systemic organ injury leads to disruption of normal systemic organ metabolic processes, which are manifest clinically by signs of accelerated anaerobic metabolism (e.g., tissue acidosis and hyperlactatemia) and altered VO2-DO2 relationships. The association of increased anaerobic metabolism with VO2-DO2 alterations has led to the notion that ischemia/ reperfusion (I/R) injury may be a prerequisite for the development of VO2-DO2 alterations during endotoxemia. However, in contrast to sepsis, in which oxygen consumption is often increased, oxygen consumption is severely decreased after I/R injury. Based on these observations, we hypothesized that I/R injury would result in systemic organ VO2-DO2 alterations, which are distinct from those that occur in sepsis.
  
  
  METHODS
  We used the in situ autoperfused feline ileal preparation to simultaneously examine microvascular permeability, reflected as the ileal lymph to plasma protein concentration ratio (CL/CP), and ileal VO2-DO2 relationships after either intravenous LPS (2.0 mg/kg; n = 5) or I/R injury (n = 5), and in matching controls (n = 5).
  
  
  RESULTS
  As expected, all LPS-treated and I/R-injured animals were found to have extensive ileal histological damage and marked increases in the CL/CP compared with controls (0.315 +/- 0.009 and 0.329 +/- 0.034, respectively, v 0.097 +/- 0.009; P < .001, both comparisons). In addition, the critical DO2 (DO2c) was elevated, and the critical oxygen extraction was decreased in both the I/R and LPS groups relative to controls. However, as initially hypothesized, the VO2 at the critical DO2 was markedly decreased in the I/R group compared with that of the LPS group.
  
  
  CONCLUSIONS
  These data indicate that I/R injury is insufficient to account for the systemic organ VO2-DO2 alterations that occur with LPS injury.
authors.affiliation: Department of Internal Medicine, Ohio State University, Columbus, USA.
authors.forename: E D
authors.initials: ED
authors.lastname: Crouser
authors.forename: M W
authors.initials: MW
authors.lastname: Julian
authors.forename: S E
authors.initials: SE
authors.lastname: Weisbrode
authors.forename: P M
authors.initials: PM
authors.lastname: Dorinsky
mesh_terms: D000138:Acidosis / Q000503:physiopathology; D000818:Animals; D002415:Cats; D019446:Endotoxemia / Q000150:complications / Q000503:physiopathology*; D006439:Hemodynamics; D007082:Ileum / Q000098:blood supply* / Q000503:physiopathology; D008297:Male; D010101:Oxygen Consumption; D015427:Reperfusion Injury / Q000150:complications / Q000503:physiopathology*